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Exercise Science Department, Arizona State University, Tempe, Arizona 85287-0404
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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This
study tested the hypothesis that women would have blunted physiological
responses to acute hypoxic exercise compared with men. Fourteen
women taking oral contraceptives (28 ± 0.9 yr of age) and 15 men
(30 ± 1.0 yr of age) with similar peak O2 consumption
(
O2 peak) values (56 ± 1.1 vs.
57 ± 0.8 ml · kg fat-free
mass
1 · min1) were studied under
hypoxic (H; fraction of inspired oxygen = 13%) vs. normoxic
(fraction of inspired oxygen = 20.93%) conditions. Cardiopulmonary, metabolic, and neuroendocrine measures were taken before, during, and 30 min after three 5-min consecutive workloads at
30, 45, and 60% O2 peak. In women
compared with men, glucose levels were greater during recovery from H
(P < 0.05) and lactate levels were lower at 45%
O2 peak, 60%
O2 peak, and up to 20 min of recovery
(P < 0.05), regardless of trial (P < 0.0001). Although the women had greater baseline levels of cortisol and
growth hormone (P < 0.0001), gender did not affect
these hormones during H or exercise. Catecholamine responses to H were
also similar between genders. Thus the endocrine response to hypoxia
per se was not blunted in women as we had hypothesized. Other
mechanisms must be at play to cause the gender differences in metabolic
substrates in response to hypoxia.
catecholamines; cortisol; metabolites
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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LIMITED RESEARCH HAS
EXAMINED the impact of gender on hormonal and metabolic responses
to acute hypoxic exercise. Recent extensive studies have examined the
effects of chronic hypoxia in women during different phases of the
menstrual cycle (2, 3, 24). However, these studies were
not examining the impact of gender per se, because they lacked a
comparably fit male control group. Nevertheless, metabolic differences
do seem to exist after acclimatization to 4,300 m, with women shifting
toward greater fat (3) and men shifting toward greater
carbohydrate use (29) during exercise. In normoxia
(
1,500 m), gender does alter the sympathetic and metabolic responses
to prolonged (8, 15, 33) and supramaximal exercise
(11). For example, women have a greater reliance on fat
oxidation and a blunted plasma catecholamine response during exercise
at the same relative intensity compared with men with similar fitness levels (8, 11, 15, 33). In addition, women, compared with men, also have a reduced plasma catecholamine response to hypoglycemic (7) and cognitive stressors
(21), possibly due to a direct inhibitory effect of
estradiol on the sympathetic nervous system (SNS) (6). Yet
it remains unknown whether plasma catecholamine responses differ
between comparably fit men and women during acute hypoxic exercise. It
seems plausible that SNS response to the stress of acute hypoxic
exercise will also be different between genders, with the prediction
that women will have a lower plasma catecholamine response compared
with men.
The hypothalamic-pituitary-adrenal (HPA) axis is also stimulated in response to stress and, therefore, can influence fuel availability (9). Animal studies suggest a potential stimulatory effect of estradiol and/or progesterone on the HPA axis at rest (4), and this suggests that women have an enhanced responsiveness of the HPA axis compared with men. However, in response to prolonged exercise, Davis et al. (8) and Horton et al. (15) found no differences in cortisol responses between men and women. Exercise under hypoxic vs. normoxic conditions causes greater increases in cortisol levels for a given workload in both men (32) and women (3). However, it remains to be determined whether the magnitude of this response to hypoxic exercise is different between comparably fit men and women.
The purpose of this study was to compare the endocrine and metabolic responses to hypoxic exercise in similarly fit men and women exposed to acute hypoxic exercise under the same experimental conditions. We hypothesized that, because of reduced SNS drive in response to hypoxic exercise, women would have significantly lower plasma catecholamines and, consequently, lower cardiorespiratory, glucose, and lactate, but greater cortisol responses to hypoxic exercise compared with men. Because of the SNS inhibitory effects on insulin and stimulatory effects on growth hormone, we also predicted that the men would have lower insulin but greater growth hormone response to hypoxic exercise compared with women.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subject Recruitment
Young (20-35 yr of age), healthy, recreationally active women taking oral contraceptives (OC; n = 14) and men (n = 15) were recruited for this study (Table 1). Women taking OC were recruited to control the hormonal fluctuations of the normal menstrual cycle and because this is the subject pool in which differences have been previously found (31). Because fitness (20) and body fat can affect the sympathetic response to exercise, only subjects with a peak O2 consumption (O2 peak) of 40-50 ml · kg fat-free mass1 · min1 and average
percent body fat [23% for women and 15% for men as classified by
Heyward (14)] were accepted into the study. O2 peak is expressed relative to
fat-free mass to control fitness for differences in body composition.
All subjects signed an informed consent approved by the Institutional
Review Board at Arizona State University.
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Preliminary Assessments
Before or during participation in this study, subjects reported no exposure to an altitude of >3,000 m within 1 mo before each trial, no history of severe acute mountain sickness, no problems associated with venipuncture, and no medications taken during the experimental trials (besides OC). All female subjects had been taking OC for at least 6 mo before participating in the study and were taking OC for birth control reasons rather than for menstrual cycle regulation.Body composition analysis was assessed via the skinfold technique using a three-site skinfold equation appropriate for gender [Jackson et al. (17) for men and Jackson and Polluck (16) for women]. Body density was converted to percent body fat using the appropriate age- and gender-specific equation (14).
O2 peak was measured on a cycle
ergometer using a continuous incremental protocol starting at 50 W,
with increases in workload by equal increments every 2 min to
exhaustion. Respiratory gas exchange data were collected
continuously using a Parvo Medics True Max metabolic cart (Consentius
Technologies, Sandy, UT). Heart rate was recorded every 5 s with a
Polar Vantage XL heart rate monitor (Polar Electro, Port Washington,
NY), and the data were downloaded onto a computer for further analysis.
All subjects met at least two of the following criteria for the
O2 peak test: respiratory exchange
ratio of 
1.1, maximum heart rate of ±10 beats/min of age-predicted
maximum (220 
age), or an increase in O2 consumption
(O2) of 150 ml/min with an increase in workload.
Exercise Protocol
Figure 1 illustrates the testing protocol. All subjects were tested on 2 different days: once while breathing room air [normoxia (N)] and once while breathing 13% oxygen [hypoxia (H)], which simulates the hypoxic effect of 2,160-m altitude. The order of H and N trials was randomized. For both men and women, the H and N trials were performed either during the same week or 4 wk apart. However, the women were always tested during the 3rd wk of their pill cycle when the effects and/or dosage of estradiol and progesterone within the OC are maximized.
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Subjects reported to the laboratory between 5 and 10 AM after an
overnight 10-h fast. On repeated trials, subjects were tested at the
same time of the morning, and an equal number of subjects in the male
and female groups were tested in late vs. early morning hours. A venous
catheter was inserted into an antecubital vein by an experienced
technician, and subjects then rested for 30 min to ensure accurate
baseline hormonal levels. Subjects then moved to the cycle ergometer
for resting and exercise data collection. An initial resting baseline
period of 10 min (B1) was conducted while subjects breathed room air
through an open-circuit system. Subjects remained seated and sedentary
on the bike for 10 more min [second baseline period (B2)]. At the
start of B2, for both trials, a short hose was connected to the
inspiratory side of the Hans Rudolph mouthpiece. This hose was then
connected to a two-way valve to allow subjects to breath either room
air (N) or from a Douglas bag that was filled with ~13%
O2 from a medical gas tank (H). After B2, the exercise
stages began and consisted of three 5-min consecutive cycling workloads
corresponding to 30 (E1), 45 (E2), and 60% of
O2 peak (E3) (equals normoxic O2 peak pedaling at ~70 rpm). Thus
subjects performed the same absolute workload in the H and N trials,
and the only difference between the trials was that subjects breathed
13% O2 from B2 through E3 during H. The exercise
intensities were chosen to maximize differences between each exercise
stage but could not exceed 60% O2 peak
because of the corresponding high relative intensity in the H trial,
which would approach hypoxic O2 peak.
An exercise duration of 5 min per stage of exercise was used to allow
us to study the effect of three different exercise intensities. Because
previous studies had shown similar arterial catecholamine levels
between 5 and 15 min of exercise (13), we felt 5 min would
be long enough to represent the endocrine response at each exercise
intensity. Recovery data were collected for 30 min postexercise while
the subject remained on the cycle ergometer breathing room air.
Measurements
Heart rate and respiratory gas exchange measurements were measured continuously throughout resting, exercise, and recovery periods with the Polar Vantage XL heart rate monitor and the Parvo Medics True Max system, respectively. Blood pressure was taken (measured manually) and blood samples were collected with 1 min left in each resting and exercise stage, and at 10 (R1), 20 (R2), and 30 min (R3) of recovery.Blood samples were analyzed for lactate levels using the YSI 1500 Sport
Lactate Analyzer (Yellow Springs Instruments, Yellow Springs, OH) or
spun in a cold centrifuge (5°C) for 15 min at 3,000 rpm. A portion of
the plasma samples was analyzed for glucose with the Beckman Glucose
Analyzer 2 (Fullerton, CA). Metabisulfite was added to a portion of
plasma samples taken at B1, B2, E1-E3, and 10 min postexercise and
were stored at 80°C for later analysis of norepinephrine and
epinephrine. The remaining plasma for each measurement period (B1
through R3) was aliquoted and stored at 80°C for subsequent
analysis of cortisol (all subjects), growth hormone, and insulin
(n = 8 each for men and women).
Cortisol, growth hormone, and insulin were analyzed using a commercially available radioimmunoassay kit (ICN Biomedicals, Costa Mesa, CA) with an intra-assay coefficient of variation of 1.99, 4.02, and 2.97% and interassay coefficient of variation of 16.3, 6.6, and 9.1% for cortisol, growth hormone, and insulin, respectively.
Catecholamines were analyzed via HPLC (ESA, Chelmsford, MA) with electrochemical detection. Briefly, 1.5 ml of plasma were combined with 10 mg of alumina (BAS). Dihydroxybensylamine was then added as an internal standard to all samples. One milliliter of 2 M Tris · EDTA buffer at pH 8.7 was added to samples to facilitate binding of catecholamines to the alumina, and the vials were then shaken for 15 min. The plasma layer was then discarded, and the alumina was washed three times with deionized and distilled water. Catecholamines were then extracted from the alumina by using 200-µl eluting agent (ESA). Samples were centrifuged at 2,000 rpm for 3 min. Fifty microliters of eluant were then injected into the HPLC column (ESA) for analysis. The interassay coefficient of variation for catecholamine analysis was 19%.
Lactate Threshold Test
Based on the finding that lactate levels were quite variable for a given exercise intensity relative to maximal O2 consumption (O2 max), it has been
suggested that exercise intensity should be expressed relative to the
lactate threshold rather than as a percentage of
O2 max (27). Because of
this potential impact on our results and because it is unknown whether
gender can impact the lactate threshold, a subset of subjects
(n = 14: 7 men and 7 women) returned to the laboratory
for a lactate threshold test. Data between genders could then be
compared relative to the lactate threshold, relative to
O2 peak, and with regards to the
absolute workload performed. Subjects reported to the laboratory
between 6 and 9 AM after an overnight fast. Again, men were tested
anytime of the month, and women were tested during the 3rd wk of their
pill cycle. A venous catheter was inserted into an antecubital vein,
and subjects then rested for 30 min for accurate baseline hormonal
levels. Subjects then moved to the cycle ergometer for resting and
exercise data collection. An initial resting baseline period of 10 min
was conducted while subjects breathed room air through an open-circuit
system. The exercise stages then began and consisted of increments of
12.5% of maximum workload (determined from previous
O2 peak protocol) every 2 min to exhaustion.
Heart rate and respiratory gas exchange measurements were measured continuously with the Polar Vantage XL heart rate monitor (Polar Electro) and the Parvo Medics True Max system (Consentius Technologies), respectively. Blood samples were collected, and ratings of perceived exertion were measured within the last 30 s of the resting and exercise stages. Blood lactate was analyzed using the YSI 1500 Sport Lactate Analyzer (Yellow Springs Instruments).
Determination of the Lactate Threshold
The lactate threshold was determined for each individual subject by plotting relative exercise intensity against lactate. Regression analysis was then used to estimate the intensity characterized by a nonlinear increase in lactate (12). This is done by performing separate linear regression analyses on the lactate vs.O2 plot for the first three, four, five,
and so on, up to eight data points representing each stage of the
O2 peak test. The lactate threshold was
reflected by a decrease in the R2 and an
increase in lactate concentration (nonlinear rise) at the next exercise stage.
Statistical Analysis
All variables were analyzed with a three-way analysis of variance for time (B1 through R3), trial (H and N), and group (men vs. women). All potential interactions were tested, but only significant interactions are reported. Paired contrasts were used as a post hoc test to identify significant differences. Using the change in heart rate during H and N exercise from a pilot study using a similar protocol with
= 0.05 and 
= 0.80, we estimated that the number of subjects needed to detect a 20% difference in heart rate
is 14 per group (men vs. women).
The mean lactate threshold value for the men and women was
statistically compared using an unpaired t-test. Statistical
significance for all tests was accepted at P 0.05.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Physical Characteristics
Because of the experimental design, there were no gender differences in age orO2 peak relative
to fat-free mass (Table 1). There were also no significant
differences in fat mass. However, the men had a higher body mass index,
fat-free mass, and a greater absolute and relative (to total body mass) O2 peak (Table 1). Subjects were
recreational runners, cyclists, triathletes, and/or mountaineers.
The OC brand name, type of synthetic estradiol and progestin, and
length of time on OC for each female subject are listed in Table
2. Most subjects were taking a monophasic
pill preparation, which had a constant dosage of estradiol and
progestin for 3 wk and placebo for 1 wk. Three subjects were taking a
triphasic pill preparation, which contained a constant dosage of
estradiol but progressively increased the progestin dosage each week
until the placebo week.
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Cardiopulmonary Variables
Cardiovascular.
Heart rate was greater in H vs. N at all time points except B1
(trial × time interaction, P < 0.0001; Fig.
2). As expected, mean arterial pressure
increased (main effect of time; P < 0.0001; Fig.
2B) during exercise workloads vs. baseline and recovery time points.
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Respiratory.
H caused a greater increase in ventilation compared with N, and this
increase was greater in men vs. women during all exercise time points
(gender × time × trial interaction; P = 0.009; Fig. 3A). When
expressed relative to fat-free mass (to control for gender differences
in body size), H still caused a significantly greater ventilatory
response at B2 and during and 10 min after exercise time points
(trial × time interaction; P < 0.0001; Fig. 3B). However, the gender difference during H was gone, but
during N the women had greater ventilatory responses compared with the men (trial × gender interaction; P = 0.002; Fig.
3B).
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Metabolic Variables
Gas exchange.
As expected, absolute O2 significantly
increased with exercise in H (trial × time; P < 0.0001) and was significantly greater in men vs. women (gender × time; P < 0.0001; Fig. 3C). When expressed relative to fat-free mass, O2 still
increased with exercise and was greater in H vs. N (trial × time
interaction; P < 0.001; Fig. 3D), but there
was no longer an effect of gender (P = 0.63).
Glucose.
The women had lower glucose levels at baseline and the first exercise
workload (E1) in H and N but had greater glucose levels during recovery
from H vs. the men (gender × trial × time interaction; P = 0.04; Fig.
4A). Because baseline
differences existed, percent change from baseline values was also
calculated. This analysis showed that glucose levels were significantly
elevated over baseline during recovery in women vs. men during H
(gender × trial × time interaction; P = 0.05; 29.8 ± 2.5, 24.3 ± 4.6, and 20.3 ± 4.7% vs.
14.8 ± 3.2, 7.4 ± 2.3, and 4.3 ± 2.3% in women vs.
men for R1, R2, and R3, respectively).
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Lactate. As expected, lactate levels increased to a greater extent in H vs. N at E2 through R3 (trial × time interaction, P < 0.0001; Fig. 4B) and was greater in men vs. women at E3 through R2 (gender × time interaction, P < 0.001; Fig. 4B).
Neuroendocrine Variables
Growth hormone.
The data for the subset of subjects (8 women and 7 men) whose plasma
samples were also analyzed for growth hormone and insulin are in Fig.
5, A and B,
respectively. Absolute growth hormone levels significantly increased at
E2, E3, and R1 compared with B1, B2, E1, R2, and R3 (main effect of
time; P < 0.0001) but were not significantly different
between trials (P = 0.89). In addition, the women had
greater growth hormone levels across all time points (main effect of
gender; P = 0.01).
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Insulin. Women had significantly greater insulin levels during H, regardless of time (gender × trial; P = 0.03), and women had significantly greater insulin levels than men at R2 and R3, regardless of trial (gender × time; P < 0.0001; Fig. 5B).
Catecholamines.
Norepinephrine levels increased with exercise (main effect of time;
E1-E3 > B1 and B2; P < 0.001; Fig.
6A) and were greater in H vs.
N across all time points (main effect of trial; P = 0.008), but there was no effect of gender (P = 0.72).
Epinephrine levels were not significantly different with time or trial
or between genders (P = 0.68, 0.55, and 0.30 for time,
trial, and gender, respectively; Fig. 6B).
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Cortisol.
Cortisol levels did not change with exercise or with H
(P = 0.4 and 0.5 for time and trial, respectively; Fig.
6C). However, across all time points and for both trials,
women had greater cortisol levels compared with men (main effect of
gender, P < 0.0001). When expressed as a percent
change from baseline, cortisol was significantly greater during H vs. N
at E3 and R1 (P = 0.03; 22.4 ± 5.3 and 22.9 ± 6.7% vs. 0.38 ± 2.9 and 3.9 ± 3.4% change from
baseline for E3 and R1, respectively, in H vs. N).
Lactate Threshold Comparisons
Physical characteristics.
Physical characteristics of this subset of subjects are summarized in
Table 3. Briefly, the men had a
higher body mass index, fat-free mass, absolute
O2 peak, and maximum workload (P < 0.05). However, there were no significant
differences between genders in percent body fat, fat mass, or
relative O2 peak (relative to
body mass and fat-free mass).
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Lactate threshold.
The lactate threshold (63.3 ± 4.7 vs. 63.4 ± 3.7%
O2 peak; P = 0.99;
Table 4) was not significantly different
between women and men when expressed at the same relative exercise
intensity. When expressed as an absolute workload, the women
had a significantly lower workload at the lactate threshold vs. the men
(135.4 ± 11.2 vs. 184.1 ± 13.9 W for women vs. men;
P = 0.02).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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This is the first study to compare comprehensively the endocrine responses to acute hypoxic exercise in similarly fit men and women. The most physiologically significant results of this study were that the men had greater lactate responses during and after hypoxic exercise, the women had greater glucose levels after hypoxic exercise, and that these differences occurred independent of endocrine responses. Thus the endocrine response to hypoxia per se was not blunted in women as we had hypothesized, yet metabolic substrates were still affected by gender.
The additional stimulus of hypoxia during exercise may override gender differences in endocrine response to normoxic exercise. At rest, muscle sympathetic nerve activity was greater in women (no control of menstrual cycle) at 3-7 min but not after 7 min of breathing hypoxic gas compared with men (28). During exercise, both with acute exposure (23) and with chronic exposure to hypoxia (10 days at 4,300 m) (3), women have similar plasma catecholamine responses as that of a group of men previously studied (25). In the acute study, the women had a greater epinephrine excretion rate (23) compared with men previously studied (25). These results support our results and suggest that women may be more sensitive to hypoxia, abolishing the blunted sympathetic response to stress seen in normoxic conditions.
There are a couple of potential caveats to this conclusion. First, plasma norepinephrine levels are susceptible to both changes in spillover from the SNS and clearance from the plasma. A previous study found that 20 min of hypoxic exercise (11% O2) caused an increase in spillover and arterial norepinephrine levels (19), suggesting that it is not decreased clearance that causes increases in norepinephrine levels found in our study and others (23). Second, despite the fact that mean epinephrine levels were over three times greater than baseline by E3, this increase was not significant. Thus the possibility exists that the present protocol did not provide enough stimulus to test differences in the sympathoadrenal system between men and women during hypoxic exercise and that differences may, in fact, exist.
The fact that subjects exercised at the same absolute workload rather
than the same percentage of O2 peak
between their H and N trials may have contributed to the lack of
difference in epinephrine between trials. However, in support of the
importance of absolute workload, the SNS has been shown to play a role
in the regulation of metabolic responses to the energy requirements of
the working muscles (5, 30). In addition, Braun et al. (3) found no significant differences in plasma epinephrine at the same relative exercise intensity and smaller differences in
plasma norepinephrine at the same relative vs. absolute exercise intensities between chronic altitude and sea-level trials. Another variable that could have contributed to the lack of epinephrine response could have been that 5 min of exercise may not be long enough
to elicit a change in plasma catecholamine levels that are reflective
of each exercise intensity. However, others have found no difference in
arterial levels of catecholamines between 5 and 15 min of exercise
(13). Future studies of acute hypoxic exposure with longer
exercise protocols, using both absolute and relative exercise
intensities and norepinephrine spillover measures, can address these issues.
Cortisol and growth hormone responses were also not blunted in women in response to H exercise. In fact, at baseline, these hormones were elevated in women vs. men. This is most likely due to estradiol. The synthetic estrogen contained within all OC preparations for subjects in this study increases hepatic synthesis of steroid binding proteins (26), causing increased total cortisol levels (1). Estrogen is also thought to increase growth hormone secretion by increasing sensitivity to pulsatile secretions of growth hormone-releasing hormone (34). However, because these hormonal responses were not different over time or with trial, these hormones are not the mechanisms for the gender differences in lactate and glucose levels.
Despite the absence of a gender effect on endocrine response, women,
compared with the men, had significantly greater glucose levels after,
and lower lactate levels during and after, H exercise. Others have also
shown similar plasma catecholamines but reduced rates of removal of
glucose after, but not during, exercise at 88%
O2 max in women during the early
follicular phase vs. men (22). Also, after chronic
exposure to hypoxia (4,300 m), women did not increase glucose rate of
disappearance, as had been previously shown in men (29)
during exercise at 65% altitude-specific O2 max.
Others who have reported lower lactate levels during prolonged (10) and supramaximal (11, 35) normoxic exercise also found lower plasma catecholamines in women vs. men. Because the present study did not find differences in plasma catecholamines in response to H exercise, other mechanisms may be at play during H to increase lactate levels during, and decrease glucose uptake after, exercise in men vs. women. One factor is the greater absolute work rates for the men (87.1 ± 2.9, 130.7 ± 4.4, and 174.2 ± 5.8 W vs. 64.2 ± 2.3, 96.4 ± 3.5, and 128.5 ± 4.6 W for E1, E2, and E3, respectively, in men vs. women; gender × time interaction; P < 0.0001). Greater workloads suggest greater energy turnover and more glycolytic flux, leading to greater lactate levels. The signals that stimulate the activation of glycogen phosphorylase to increase glycogenolysis could be inorganic phosphate and calcium, which result directly from muscle contraction. Another factor is estrogen. Administration of estrogen to rats has been shown to spare glycogen during exercise, possibly by increasing lipid availability during exercise (18). However, the route by which estrogen increases lipid availability is unknown. Regardless of the mechanism(s), if women were using less glycogen during hypoxia, they would produce less lactate during exercise. After exercise, the need for glycogen repletion would be less and might contribute to reduced removal and consequently increased plasma levels of glucose. These factors could explain why differences in metabolic responses to hypoxic exercise occurred in the absence of a blunted endocrine response to hypoxic exercise.
Based on the finding that lactate levels were quite variable for a
given exercise intensity relative to
O2 max, it has been suggested that
exercise intensity should be expressed relative to the lactate
threshold rather than as a percentage of
O2 max (27). However, the
results showed no impact of gender on the lactate threshold expressed
as %O2 max or power output per
kilogram fat-free mass (2.7 ± 0.19 vs. 2.7 ± 0.23%
O2 max in men vs. women;
P > 0.05). Despite some variability (ranges from 87.3 to 137.1% lactate threshold vs. 73.8 to 137.1% lactate threshold at
E3 in men vs. women), there was no impact of gender on the exercise
intensity for E1, E2, and E3 as expressed relative to the lactate
threshold in men vs. women (48.6 ± 3.6, 72.9 ± 5.4, 97.2 ± 7.2% lactate threshold vs. 49.0 ± 3.9, 73.5 ± 5.9, 98.0 ± 7.9% lactate threshold in men vs. women for E1, E2,
and E3, respectively; P > 0.05). In addition, the men
and women were consuming the same amount of oxygen per kilogram
fat-free mass, reflecting very similar relative exercise intensities.
Thus the gender differences in this study were most likely not due to
the fact that exercise intensity was expressed relative to
O2 peak.
The female subjects in this study were all taking OC so that we could
avoid the complications of studying women during the menstrual cycle.
Because of the difficulty in recruiting subjects, the brand or length
of time taking OC was assessed but not controlled. All OC prescriptions
used by the subjects in this study contained ethinyl estradiol as the
synthetic estrogen, albeit at different dosages in some cases. Estrogen
and progestin dosage within each OC may have an independent impact on
hormonal and metabolic response to exercise. However, there were no
correlations between baseline cortisol and growth hormone levels and
length of time on the pill (r = 0.35 and 0.64, respectively) and estrogen (r = 0.23 and 0.01, respectively) or progesterone (r = 0.57 and 0.05, respectively) dosage (P > 0.05 for all correlations).
Thus the wide range of time on, and types of, OC prescriptions may not
have added any more variation than studying women in different phases
of the menstrual cycle when there is wide individual variation in
reproductive hormonal levels and sensitivities, yet studying these
women added the convenience and ease of OC phase differentiation.
In summary, in contrast to our hypothesis, the women did not have a blunted endocrine response to hypoxia. However, the women did have a lower lactate during hypoxia and greater glucose response during recovery from hypoxia. These differences are most likely due to differences in absolute workload or the presence of estrogen in women vs. men. Less absolute work would lead to less lactate production and glycogen use, and thus less glucose would be taken up by the muscle for refueling glycogen stores after exercise in women. Therefore, the most significant impact of gender on the response to hypoxic exercise may be due to differences in muscle metabolism independent of endocrine drive.
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ACKNOWLEDGEMENTS |
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We thank Jeffrey Thresher and Pam Bosch for technical assistance during data collection and analysis. Special thanks to Drs. M. Pagliassotti and R. Roach for critical review of the manuscript. Also, we thank all the research subjects who volunteered to be a part of this study.
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FOOTNOTES |
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This work was supported in part by the American College of Sports Medicine-National Aeronautics and Space Administration Space Physiology Student Research Grant.
Address for reprint requests and other correspondence: D. A. Sandoval, Division of Diabetes, Endocrinology, and Metabolism, 715 Preston Research Bldg., Nashville, TN 37232-6303 (E-mail: darleen.sandoval{at}mcmail.vanderbilt.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
10.1152/japplphysiol.00526.2001
Received 2 May 2001; accepted in final form 18 September 2001.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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P < 0.0001). Values are expressed
as means ± SE. Symbols are occluding error bars where none are
visible. bpm, Beats/min. B1 through R3 are as defined in Fig.
